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Objectives: Psychosocial stressors at work have been proposed as modifiable risk factors for mild cognitive impairment (MCI). This study aimed to evaluate the effect of cumulative exposure to psychosocial stressors at work on cognitive function., Methods: This study was conducted among 9188 white-collar workers recruited in 1991-1993 (T1), with follow-ups 8 (T2) and 24 years later (T3). After excluding death, losses to follow-up and retirees at T2, 5728 participants were included. Psychosocial stressors at work were measured according to the Karasek's questionnaire. Global cognitive function was measured with the Montreal Cognitive Assessment. Cumulative exposures to low psychological demand, low job control, passive job and high strain job were evaluated using marginal structural models including multiple imputation and inverse probability of censoring weighting., Results: In men, cumulative exposures (T1 and T2) to low psychological demand, low job control or passive job were associated with higher prevalences of more severe presentation of MCI (MSMCI) at T3 (Prevalence ratios (PRs) and 95% CIs of 1.50 (1.16 to 1.94); 1.38 (1.07 to 1.79) and 1.55 (1.20 to 2.00), respectively), but not with milder presentation of MCI. In women, only exposure to low psychological demand or passive job at T2 was associated with higher prevalences of MSMCI at T3 (PRs and 95% CI of 1.39 (0.97 to 1.99) and 1.29 (0.94 to 1.76), respectively)., Conclusions: These results support the deleterious effect of a low stimulating job on cognitive function and the cognitive reserve theory. Psychosocial stressors at work could be part of the effort for the primary prevention of cognitive decline., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2021. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Chronic low-grade inflammation has been associated with high risk of several chronic diseases such as cardiovascular diseases, diabetes, depression, and dementia. As low-grade inflammation could be present long before the apparition of the disease, identifying modifiable risk factors could allow to act upstream. Psychosocial stressors at work have been suggested as modifiable risk factors of low-grade inflammation, but few longitudinal studies have evaluated the association between these stressors and inflammatory biomarkers, such as C-reactive protein (CRP) and interleukin-6 (IL-6)., Objective: This longitudinal study evaluate the associations between exposure to psychosocial stressors at work and CRP and IL-6, separately and combined into an inflammatory index., Methods: Data came from a cohort of 9188 white-collar workers recruited in 1991-1993 (T1) and followed-up after 8 (T2, 1999-2000) and 24 (T3, 2015-2018) years. Participants included in this study were randomly selected at T3 for serum biomarkers studies (n = 2557). CRP and IL-6 were measured using standardized protocols. Psychosocial stressors at work were assessed at T2 according to recognized models: Karasek's Demand-Control-Support model and Siegrist's Effort-Reward Imbalance (ERI) model, using validated questionnaires. High job strain was defined by an exposure to high psychological demand combined with low job control, and iso-strain was defined by an exposure to high job strain combined with low social support at work. ERI was defined by an imbalance between psychological demand and social, economic, and organizational reward. Several covariates were considered including sociodemographic, anthropometric, and lifestyle characteristics, and comorbidities. Prevalence ratios (PRs) and 95% confidence interval (CI) for the highest quartile of CRP, IL-6 and inflammatory index at T3 according to psychosocial stressors at work measured at T2 were calculated using generalized estimating equations. Multiple imputation and inverse probability of censoring weighting were done., Results: In men, an association was observed between exposure to iso-strain and the inflammatory index (PR of 1.42 (95% CI: 1.06;1.90)), mainly among men aged less than 65 years (PR of 2.00 (95% CI: 1.37;2.92)). In this same age group, associations with inflammatory biomarkers were also observed among men with exposure to ERI, and among women with exposure to low reward at work or moderate social support at work., Conclusion: These results suggest that psychosocial stressors at work may increase low-grade inflammation. However, further studies are needed to corroborate these results and to clarify the potential differences between men and women. As these stressors are frequent and modifiable, their reduction is important for public health and could play a role in the primary prevention of chronic diseases., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

There is growing evidence that cardiovascular health can be affected by exposure to methylmercury (MeHg), by a mechanism involving oxidative stress. Paraoxonase 1 (PON1) is a high-density lipoprotein-bound enzyme that hydrolyzes toxic oxidized lipids and protects against cardiovascular diseases. Evidence from in vitro studies indicates that MeHg can inhibit PON1 activity but little is known regarding this effect in humans. We investigated whether increased blood mercury levels are associated with decreased serum PON1 activity in Cree people who are exposed to MeHg by fish consumption. We conducted a multi-community study of 881 Cree adults living in Eastern James Bay communities (Canada). Multivariate analyses considered sociodemographic, anthropometric, clinical, dietary and lifestyle variables and six PON1 gene variants (rs705379 (-108C/T), rs662 (Q192R), rs854560 (L55M), rs854572 (-909C/G), rs854571 (-832C/T) and rs705381 (-162C/T)). In a multiple regression model adjusted for all potential confounding factors and the rs854560 PON1 variant, a statistically significant MeHg*rs705379 interaction was observed. Blood mercury levels were inversely associated with serum PON1 activities in individual homozygous for the -108T allele (P=0.009). Our results suggest a gene-environment interaction between the rs705379 polymorphism and MeHg exposure on PON1 activity levels in this aboriginal population. This finding will need to be replicated in other population studies.

Background: The increasing consumption of sugar worldwide seems to lead to several health problems, including some types of cancer. While some studies reported a positive association between sweet foods intake and breast cancer risk, little is known about their relation to mammographic density (MD), a strong breast cancer risk factor. This study examined the association of sweet foods and drinks intake with MD among 776 premenopausal and 779 postmenopausal women recruited at mammography., Methods: A food-frequency questionnaire was used to assess intake of sweet foods, sugar-sweetened beverages and spoonsful of sugar added. Percent and absolute breast density were estimated using a computer-assisted method. Multivariate generalized linear models were used to evaluate associations. All models were adjusted for potential confounders, including age and body mass index., Results: For increasing quartiles of sugar-sweetened beverages intake, adjusted-mean absolute density was respectively 32, 34, 32 and 36 cm2 among all women (P(trend) = 0.040) and 43, 46, 44 and 51 cm2 among premenopausal women (P(trend) = 0.007). For increasing quartiles of sweet foods intake, adjusted-mean percent density was respectively 16, 16, 17 and 19% among postmenopausal women (P(trend) = 0.036). No association was shown between intake of spoonsful of sugar added and MD., Conclusion: Our results suggest that an increase in sweet foods or sugar-sweetened beverage intake is associated with higher MD.

Purpose: Omega-3 (n-3) and n-6 fatty acids (FA) intake could influence the occurrence of certain diseases such as breast cancer but little is known about their relation to mammographic density (MD). The purpose of this study is to examine the association of the intake of n-3 FA and n-6 FA with MD among 777 premenopausal and 783 postmenopausal women., Methods: In this cross-sectional study, FA intake was assessed with a self-administered food-frequency questionnaire and MD was measured using a computer-assisted method. Multivariate analyses were performed by using generalized linear models to evaluate the associations of quartiles of FA intake with MD., Results: For increasing quartiles of total long-chain n-3 FA intake (< 0.11, 0.11-0.20, 0.21-0.32, and ≥ 0.33 g/day), adjusted mean MD was 29, 29, 27, and 25 %, respectively (P trend = 0.005). This association remained significant among postmenopausal (P trend = 0.006) but not among premenopausal (P trend = 0.21) women. No significant association was found between n-6 FA intake and MD. However, for increasing quartiles of the n-6 FA/long-chain n-3 FA ratio intake (< 31.75, 31.75-52.28, 52.29-94.28, and ≥ 94.29), adjusted mean MD was 26, 27, 29, and 29 %, respectively (P trend = 0.008)., Conclusions: Higher intake of long-chain n-3 FA was associated with lower MD, suggesting that increased long-chain n-3 FA intake could be a strategy for breast cancer prevention.

Background: Single nucleotide polymorphisms (SNPs) in genes involved in the estrogen pathway appear to be associated with breast cancer risk and possibly with mammographic density (MD), but little is known of these associations among premenopausal women. This study examines the association of 11 polymorphisms in five estrogen-related genes (estrogen receptors alpha and beta (ERα, ERβ), 17β-hydroxysteroid dehydrogenase 1 (HSD17B1), catechol-O-methyltransferase (COMT), cytochrome P450 1B1 (CYP1B1)) with premenopausal MD. Effect modification of four estrogen-related factors (parity, age at menarche, hormonal derivatives use and body mass index (BMI)) on this relation is also assessed., Methods: Polymorphisms were genotyped in 741 premenopausal Caucasian women whose MD was measured in absolute density (AD, cm²) and percent density using a computer-assisted method. Multivariate linear models were used to examine the associations (P(trend)) and interactions (Pi)., Results: None of the SNPs showed a statistically significant association with AD. However, each additional rare allele of rs1056836 CYP1B1 was associated with a reduction in AD among nulliparous women (P(trend) = 0.004), while no association was observed among parous women (P(trend) = 0.62; Pi = 0.02). An increase in the number of rare alleles of the HSD17B1 SNP (rs598126 and rs2010750) was associated with an increase in AD among women who never used hormonal derivatives (P(trend) = 0.06 and P(trend) = 0.04, respectively), but with a decrease in AD among past hormonal derivatives users (P(trend) = 0.04; Pi = 0.02 and P(trend) = 0.08; Pi = 0.01, respectively). Moreover, a negative association of rs598126 HSD17B1 SNP with AD was observed among women with higher BMI (>median) (P(trend) = 0.01; Pi = 0.02). A negative association between an increased number of rare alleles of COMT rs4680 SNP and AD was limited to women who never used hormonal derivatives (P(trend) = 0.02; Pi = 0.03) or with late age at menarche (>median) (P(trend) = 0.03; Pi = 0.02). No significant association was observed between polymorphisms in the ERα or ERβ genes and AD. Similar results, although less significant, were observed when MD was assessed in percent density., Conclusion: SNPs located in CYP1B1, COMT or HSD17B1 genes seem to be associated with MD in some strata of estrogen-related factors. Our findings suggest that modifying effects of estrogen-related factors should be considered when evaluating associations of polymorphisms in estrogen-related genes with premenopausal mammographic density.

Background: The effect of multivitamin-multimineral supplements on the occurrence of chronic diseases, such as breast cancer, is unclear. Breast density is increasingly used as a biomarker of breast cancer risk., Objective: The present study evaluated the association of multivitamin-multimineral supplement use with breast density., Design: Premenopausal (n = 777) and postmenopausal (n = 783) women were recruited at the time of screening mammography. Anthropometric measurements were taken at recruitment. Demographic characteristics, behavioral factors, and health conditions were documented by telephone interview. Diet and multivitamin-multimineral and individual vitamin and mineral supplement use were assessed with a self-administered food-frequency questionnaire. Breast density from screening mammograms was measured using a computer-assisted method. Crude and adjusted means in breast density were evaluated according to multivitamin-multimineral supplement use using generalized linear models., Results: Current multivitamin-multimineral supplement use was reported by 21.7% of women (20.7% and 22.6% of premenopausal and postmenopausal women, respectively). Premenopausal women who were currently using multivitamin-multimineral supplements had higher adjusted mean breast density (45.5%) than past (42.9%) or never (40.2%) users (P for heterogeneity = 0.03, P for trend = 0.009). Of the current users, breast density was not related to duration of multivitamin-multimineral supplement use. In postmenopausal women, multivitamin-multimineral supplement use was not associated with breast density (P for heterogeneity = 0.53, P for trend = 0.40)., Conclusion: Regular use of multivitamin-multimineral supplements may be associated with higher mean breast density among premenopausal women. The relations of multivitamin-multimineral supplement use to breast density and breast cancer risk need to be clarified.

In Quebec, cancer is the principal cause of mortality. This epidemiologic research program includes two components. The first component takes place at the "Institut national de santé publique du Québec" and involves surveillance and evaluation of practices in oncology with the aim of providing the Quebec Ministry of Health with some of the evidence needed to determine its policies in cancer control. The second component takes place at the "Unité de recherche en santé des populations (URESP)" of Laval University and is devoted to studying the etiology and prevention of breast cancer. This paper focuses on this second research component which uses mammographic breast density as an intermediate biomarker to study the causes of breast cancer and strategies to prevent it. Breast cancer risk is much higher among women with very dense breasts than among those with little or no breast density. Recently, we were among the first to show that women with high vitamin D or calcium intakes have less breast density than those with low intakes, especially among premenopausal women. Furthermore, we have confirmed that breast density was increased among premenopausal women with high levels of IGF-I and low levels of IGFBP3 which is consistent with the observed effect of these molecules on breast cancer risk. Studies are now being conducted to assess whether breast density varies according to blood levels of vitamin D and of additional growth factors, as well as to genetic polymorphisms involved in the pathways of vitamin D, calcium and growth factors. The increase in vitamin D and calcium intakes may prove to be a safe and inexpensive approach to breast cancer prevention; this possibility should be carefully examined as quickly as possible.